Further Inpatient Care
Pulmonary toilet
As with many diseases, the use of chest physiotherapy is widely accepted in inhalation injury but remains unproven in controlled trials. The use of percutaneous cupping and postural drainage seem reasonable to clear airways of cellular debris and soot, thereby preventing atelectasis and obstruction. Obviously, care must be taken in attempting this in the presence of significant chest wall burns.
Encourage extubated patients to cough and deep breathe. In patients who are intubated, use gentle suctioning to remove mucus, debris, and sloughed epithelium. Fiberoptic bronchoscopy may be helpful in removing the debris and in facilitating pulmonary toilet.
Mechanical ventilation with positive end expiratory pressure
With declining lung function, oxygenation, and ventilation, mechanical ventilation with positive end expiratory pressure (PEEP) may be necessary.
PEEP may assist in opening obstructed closed alveoli and help ventilation in those patients with poor compliance by increasing functional residual capacity. Ideally, PEEP stents alveoli open, preventing the atelectasis and alveolar flooding that can result from surfactant dysfunction, increasing interstitial fluid, and third-spacing.
Tracheostomy
The timing of tracheostomy continues to be controversial.[7] Certainly, in children in whom endotracheal intubation is not possible because of severe airway edema or burns, tracheostomy can be lifesaving. With early recognition of upper airway injury, this should be a rare occurrence.
Tracheostomy, especially through burned tissue, has an increased complication rate and risk of sepsis when compared with endotracheal intubation. Thus, most patients can be effectively managed with endotracheal intubation through the mouth or nose.
In patients expected to have a long period of convalescence because of severe neurologic or pulmonary injury, tracheostomy may be desirable for patient comfort and is easy to maintain.
Further Outpatient Care
After recovery from the initial injury, closely monitor those patients with residual airway obstruction and pulmonary damage. Refer patients with ongoing symptoms to a pediatric pulmonologist.
Deterrence/Prevention
Primary prevention with functioning fire and smoke alarms and family education for fire hazards is critical to help avoid fire injuries. View prevention as the primary means to avoid inhalation injury and the use of smoke and CO detectors should be encouraged community-wide.
Complications
Severe pulmonary injury, edema, and the inability to oxygenate or ventilate can result in death. Concurrent CO poisoning and inhalation of other products of combustion can cause hypoxemia, end organ injury, and morbidity.
Prognosis
Most inhalation injuries are self-limited and resolve within 48-72 hours. The severity of direct pulmonary parenchymal injury depends on the extent of exposure and the type of inhaled toxins produced during combustion. Most patients do not manifest spirometry changes. Rare long-term sequelae include tracheal stenosis, bronchiectasis, interstitial fibrosis, and bronchiolitis obliterans.
Patient Education
Programs aimed at educating young children about the dangers of playing with lighters and matches and programs teaching families how to safely escape from burning buildings should be used to further limit the number of children experiencing inhalation and burn injury. Anticipatory guidance during well child visits should include fire safety instructions.
For patient education resources, see the Lung and Airway Center, Procedures Center and Poisoning Center, as well as Smoke Inhalation, Bronchoscopy and Carbon Monoxide Poisoning.
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| Type | Inhalant | Source | Injury/Mechanism |
| Irritant gases | Ammonia | Fertilizer, refrigerant, manufacturing of dyes, plastics, nylon | Upper airway epithelial damage |
| Chlorine | Bleaching agent, sewage and water disinfectant, cleansing products | Lower airway epithelial damage | |
| Sulfur dioxide | Combustion of coal, oil, cooking fuel, smelting | Upper airway epithelial damage | |
| Nitrogen dioxide | Combustion of diesel, welding, manufacturing of dyes, lacquers, wall paper | Terminal airway epithelial damage | |
| Asphyxiants | Carbon monoxide* | Combustion of weeds, coal, gas, heaters | Competes for oxygen sites on hemoglobin, myoglobin, heme-containing intracellular proteins |
| Hydrogen cyanide† | Burning of polyurethane, nitrocellulose (silk, nylon, wool) | Tissue asphyxiation by inhibiting intracellular cytochrome oxidase activity, inhibits ATP production, leads to cellular anoxia | |
| Hydrogen sulfide‡ | Sewage treatment facility, volcanic gases, coal mines, natural hot springs | Similar to cyanide, tissue asphyxiant by inhibition of cytochrome oxidase, leads to disruption of electron transport chain, results in anaerobic metabolism | |
| Systemic toxins | Hydrocarbons | Inhalant abuse (toluene, benzene, Freon); aerosols; glue; gasoline; nail polish remover; typewriter correction fluid; ingestion of petroleum solvents, kerosene, liquid polishes | CNS narcosis, anesthetic stats, diffuse GI symptoms, peripheral neuropathy with weakness, coma, sudden death, chemical pneumonitis, CNS abnormalities, GI irritation, cardiomyopathy, renal toxicity |
| Organophosphates | Insecticides, nerve gases | Blocks acetylcholinesterase, cholinergic crisis with increased acetylcholine | |
| Metal fumes | Metal oxides of zinc, copper, magnesium, jewelry making | Flulike symptoms, fever, myalgia, weakness | |
| * Major component of smoke † Smells like almonds, component of smoke from fires ‡ Smells like rotten eggs | |||
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